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Ketan Patel, MD, FAAEM Director of Clinical Education·Disclaimer: This blog post is based on a 2015 article chosen for the Lifelong Learning and Self Assessment (LLSA) for Emergency Physicians. This blog post is in no way designed to help facilitate passing of the LLSA exam. Rather, it highlights important literature flagged as relevant to clinical practice and is thus presented here as educational material for training residents. Clinical question: What is the best way approach and manage a patient with a tachycardia presenting to the emergency department?

In order to answer this clinical question, this blog post will highlight teachings from the following 2015 LLSA article: Link MS. Clinical practice. Evaluation and initial treatment of supraventricular tachycardia. N Engl J Med. 2012:367(15):1438-48. Article can be downloaded via the following link: http://www.uphs.upenn.edu/ppmc_emergency/PPMC%20Bookmarks/2015%20LLSA%20Articles/Supraventricular%20Tachycardia.pdf The first part of this article focuses on characteristics of various atrial tachycardias (along with premature atrial complexes). The latter half of the articles discusses strategies in identifying these tachycardias, differentiating them from ventricular tachycardias and a management algorithm for patient treatment. This article has great table, which summarizes the differential diagnosis of supra ventricular tachycardias (SVTs) with rhythm strip examples, causes, regularity, average rates, and response to adenosine. I have summarized some of this data below for completeness, but please reference the article for this information as it a great concise look at SVTs. Characteristics of various atrial tachycardias: Regular SVTs: 1.Sinus tachycardia

Most common SVT. Not pathologic, but an appropriate response to some stressor. It is gradual in onset and recession. The rate typically does not go above 220 beats per minute (BPM). Being a regular rhythm, P waves precede the QRS complex.

2.Atrial flutter (AF)

2nd most common pathologic SVT with rapid onset. A reentrant circuit in the right atrium causes a regular rhythm with a atrial rate of 280 to 300 bpm. When a 2:1 conduction is present in the atrioventricular node (AV node), the ventricular rate is 140 to 150 bpm.

3.AV nodal reentrant tachycardia (AVNRT)

Rapid onset, 150-250 bpm. Abnormal electrical circuits is the culprit. Patients are usually in their 20’s.

Caused by a reentrant loop between the AV node and atrial tissue. You get simultaneous depolarization of the atrium and ventricle as the electrical impulse goes from forward from the AV node to ventricle and a impulse goes retrograde through a slow pathway from the AV node to the atrium. As a result, P waves are usually absent on the EKG.

Caused by bypass tracts between atria and ventricle. Can conduct through these tracts anterograde, retrograde or bidirectional. In most anterograde conductions, delta waves are present on EKG. A tachycardia with a delta wave confirms Wolff-Parkinson-White syndrome.

i.Orthodromic conduction: down the AV node and retrograde conduction via the bypass. Narrow and regular QRS.ii.Antidromic: conduction down bypass and retrograde via AV node. Wide and regular.iii.Wide and irregular QRS complexes are seen in the setting of atrial fibrillation which can reulst in rapid and fatal ventricular arrhythmias. 5.Atrial tachycardia (AT)

Rapid onset, 150-250 bpm. Abnormal electrical circuits or focal arrhythmias can be the culprit. Usually have a warm-up period over 10 minutes where the rate increases before stabilizing. They may also occur in short bursts.

Irregular SVTs 1.Atrial fibrillation (AF)

Most common pathologic SVT. Multiple risk factors including coronary arterial disease and hypertension. Atrial fibrillation results from multiple electrical foci within the atria simultaneously. It can be sudden or gradual in onset. Acute onset results in patients with previous sinus rhythms that can jump up to rates of 160 bpm. In chronic AF, rapid heart rates arise gradually usually secondary to an underlying factor. In all episodes, the ventricular rate can be 60 to 220 bpm, and is irregular.

2.Atrial flutter (AF) with variable AV block

Can occur in patients with AV node disease or secondarily from medications, which causes an irregular heart rate less chaotic than atrial fibrillation.

3.Multifocal atrial tachycardia (MAT)

Multiple premature beats in atrium. Uncommon due to decreased utilization of theophylline but can still be seen in hypoxia and settings of increased atrial pressure. Gradual in onset. At least three different P wave morphologies are needed for diagnosis.

4.Multiple atrial premature contractions (not a true tachycardia but can result in a similar presentation as SVT).

Arise for a isolated focus. P wave morphology are similar to atrial tachycardia. Can be sudden or gradual and is contingent on the underlying rhythm.

Identification and Management

Differential Diagnosis 1.Focus on the ventricular rather than atrial response. Evaluate the QRS to differentiate between narrow and wide. Next, assess for regularity on the EKG and then attempt to determine if the onset was gradual or rapid. Always consider the heart rate in your determination as well. a.Narrow Complex i.Evaluation 1.P waves preceding the QRS: sinus tachyrdia, multiple atrial premature contractions. 2.P waves after WRS: AVNRT. 3.Be careful with atrial flutter of 2:1 conduction. If the rate is 150, have a high suspicion even if you don’t see a flutter wave, which may be buried in T wave.ii.Management 1.Vagal maneuvers a.Block the AV node by increasing vagal tone. If successful, the resultant decrease in heart rate can confirm a sinus tachycardia, A. Fib or A. Flutter. It can also terminate AVNRT and AVRT. 2.Adenosine a.Blocks AV nodal conduction and ceases almost all AVNRT and AVRT and majority of AT. Article notes to be careful in patients with heart transplant and when a central venous catheter is placed and to lower initial dose to 3mg. 3.Calcium channel blockers a.Block the AV node and may be helpful for diagnostic and therapeutic usage. They may cause hypotension. 4.Electrical cadioversion a.Utilized for patients who are unstable and refractory to adenosine. 5.Antiarrhythmic medications a.May use procainamide and ibutilide if patient is unstable and does not respond to cardioverison. FIGURE 3 IN THE ARTICLE PRESENTS AN ALGORITHM FOR IDENTIFICATION AND MANAGEMENT OF NARROW-COMPLEX TACHYCARDIAS. b.Wide complex i.Be cautious as these may be ventricular arrhythmias or SVT. 1.Regular – ventricular tachycardia or regular SVT 2.Irregular – polymorphic ventricular tachycardia, torsades de pointes, ventricular fibrillation or a irregular SVT.ii.Management 1.Adenosine a.Should only be given in regular tachycardia as medication may be associated with risk of increasing conduction through bypass tract. Can be helpful in evaluation and treatment of wide-complex regular tachycardias. 2.Calcium channel blockers a.Avoid as they can cause hypotension and death 3.Electrical cardioversion a.Utilize in unstable patients 4.Antiarrhythmic medications a.May be useful in treatment of wide-complex tachycardia ***stable wide-complex tachycardia that is irregular could be A. Fib with aberrancy or WPW. These patients should get a expert consult for management according to article. FIGURE 4 IN THE ARTICLE PRESENTS AN ALGORITHM FOR IDENTIFICATION AND MANAGEMENT OF NARROW-COMPLEX TACHYCARDIAS.

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